ArticleImmunity2026
Polystyrene microplastic-induced pathophysiology is driven by disruption of efferocytosis.
Article in Immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Article
- Microplastics inhibit macrophage bioenergetics impairing homeostatic function and immune responsiveness.bioRxiv : the preprint server for biology · 2026Article
- Pathogenesis of Micro/Nanoplastics in Mammalian Systems: Gut to Systemic Multi-Organ Dysfunction.Research (Washington, D.C.) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Microplastics (MPs), microparticles from plastic degradation, pose a substantial threat to human health. Macrophages, the body's immune sentinels, are unable to break down MPs, suggesting that MP accumulation could impair essential functions, such as removal of apoptotic cells (ACs), termed efferocytosis. We found that polystyrene MP (PS-MP) accumulation disrupted efferocytosis by impairing AC digestion in multiple types of macrophages and Sertoli cells, specialized testes phagocytes, in vitro. PS-MP exposure also suppressed efferocytosis and caused damage in the lungs, liver, and testes in vivo. Mechanistically, PS-MP-loaded efferocytotic macrophages had dysregulated metabolic and phagolysosome processes, including accumulation of methylglyoxal (MGO) and increased MGO glycation of glucose-6-phosphate dehydrogenase, an enzyme required for AC digestion. Consistently, we found that overexpression of the MGO detoxification glyoxalase-1 rescued PS-MP-induced defects in AC digestion in vitro and in vivo. Collectively, we demonstrate that PS-MPs directly disrupt efferocytosis, which negatively affects the function and health of multiple organs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.